The purpose of this project is to determine if there is an intrarenal negative feedback mechanism to control renin secretion in renal vascular hypertension in dogs and man. In previous experiments the principal investigator has demonstrated intrarenal vasoconstriction following partial renal artery occlusion, associated with this was a decrease in renin secretion. The most likely mechanism producing the vasoconstriction is the renin-angiotensin system. This work will determine if this system is producing the vasoconstriction by studying the effect of the Angiotensin II blocking agent (1-sarcolyl, 8-alanine angiotensin II) and converting enzyme inhibitor (Squibb 20881) on renal function. The role of Angiotensin II on filtration fraction will be determined with clearance techniques. If this mechanism is responsible for the vasoconstriction in the dog with renal vascular hypertension this will also be studied in other physiological conditions in the dog as well as in the man if these blocking agents become available for human use.